Biological explanation of depression Flashcards
summarise the monoamine depletion hypothesis
- depression caused by abnormally low levels of monoamine neurotransmitters e.g. serotonin, noradrenaline, dopamine.
- these neurotransmitters regulate function of limbic system which is the brain’s emotional centre.
the permissive hypothesis developed from the Monoamine depletion hypothesis - what is this?
it suggests that it is the balance of serotonin and noradrenaline that causes depression. The level of serotonin normally controls levels of noradrenaline. But low levels of serotonin cause noradrenaline to decrease as well which leads to the outcome of depression. This suggests that serotonin is a necessary factor fo causing depression but not sufficient on its own.
why was the monoamine depletion hypothesis quickly considered over-simplistic?
drugs were developed that had antidepressant properties but did not increase availability of monoamine neurotransmitters, which suggested there was more to depression than monoamine depletion.
summarise receptor sensitivity hypothesis
argued that depression is caused by changes in the sensitivity of post-synaptic receptors. In depression, serotonin and noradrenaline post synaptic receptors become even more sensitive to reduced stimulation than normal.
summarise the BDNF hypothesis
Brain derived neurotrophic factor is a chemical which feeds neurons nutrients they need in order to survive. This means it plays a large role in neuronal plasticity - the ability for the brain to form new synapses. Levels of BDNF very low in people with depression. The lower the levels, the more severe the symptoms. Therefore, allows researchers to link depression with stress. Gene for BDNF can be switched off under stress which leaves neurons fed by BDNF vulnerable to cell death (apoptosis) which is observed in depression.
what is a strength supporting the role of the BDNF
studies have found correlation between levels of BDNF and the severity of depressive symptoms. Post-mortem studies of brains of people who had depression have found low level of BDNF in hippocampus.
what are some evidence against monamine depletion
It can’t explain the common experience of therapeutic delay. When people start taking antidepressants it takes 4-6 weeks to see improvements. This delay is hard to explain when levels of serotonin and noradrenaline supposedly increase immediately after one week.
What is the counter to the evidence against monoamine depletion?
It can be explained by receptor sensitivity. Antidepressants increase the availability of serotonin in synapse. This leads to correspondingly decrease in post synaptic receptors to compensate for grater stimulation. But this process is not immediate - it takes several weeks and correlates closely with symptom improvement.
what is a weakness of neurochemical explanations?
Researchers assumed if biochemical treatment improved symptoms of depression then this implies depression must have a biochemical cause. However this is not the case as an antidepressant drug could work by correcting a biological process that is disturbed by a psychological factor (e.g. stress) so treatment is biological but the cause is psychological = treatment aetiology fallacy.
how can neuro-chemical explanation of depression have application to society.
new drug treatment creation targeting serotonin and noradrenaline level. BDNF offers an alternative route involving a different type of biological treatment (TMS) transcranial magnetic stimulation. This is a strength because treatments are based on biochemical explanations which may help improve quality of life and reduce distress in person with depression.
